BackgroundBreast cancer, the leading cause of cancer deaths among women, exhibits high heterogeneity, affecting prognosis. Understanding this heterogeneity and developing prognostic models are crucial for accurate identification of high-risk patients.MethodsAccessing breast cancer gene expression and clinical data from public datasets, we identified differential expression genes in tumor vs. non-tumor tissues using TCGA data. Key DEGs were then selected using LASSO and Cox regression, and a prognostic risk model (BRCA-DEGs-LASSO-Cox) was constructed. Survival analysis estimated model predictability, identifying high-risk patients. Correlation between risk score and signaling pathways, immune status, and drug sensitivity was analyzed. Molecular mechanisms underlying high-risk patients were discussed.ResultsOur analysis identified 1217 downregulated and 689 upregulated DEGs in breast cancer tumor tissues. A BRCA-DEGs-LASSO-Cox model was constructed using four key DEGs, stratifying patients into high/low-risk groups. High-risk patients had worse OS across cohorts and were associated with androgen, estrogen, and PI3 K signaling pathway dysregulation. They also exhibited immune status dysregulation and drug sensitivity disturbances. Molecular mechanism analysis indicated abnormal regulation of cell cycle, mitosis, and immune-related signals in high-risk patients, explaining their poorer prognosis.ConclusionsBRCA-DEGs-LASSO-Cox model effectively identifies high-risk breast cancer patients, revealing key signaling pathways, immune status, drug sensitivity, and molecular mechanisms.